Evidence map›Paper›PMID 21502359›Full record

ArticleThe Journal of cell biology2011

Isoform-specific targeting of PKA to multivesicular bodies.

Michele E Day, Guido M Gaietta, Mira Sastri, Antonius Koller, Mason R Mackey, John D Scott, Guy A Perkins, Mark H Ellisman, Susan S Taylor

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
1.6field-weighted citation impact, top 17% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
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  15. Role of A-Kinase Anchoring Protein 12 in the Central Nervous System.Journal of clinical neurology (Seoul, Korea) · 2023
    Review
  16. Review
  17. Article
  18. Cancers · 2021
    Review
  19. Selective autophagy of AKAP11 activates cAMP/PKA to fuel mitochondrial metabolism and tumor cell growth.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Michele E DayBioinformatics Program, University of California at San Diego, La Jolla, CA 92093, USA.
Guido M Gaietta
Mira Sastri
Antonius Koller
Mason R Mackey
John D Scott
Guy A Perkins
Mark H Ellisman
Susan S Taylor
Howard Hughes Medical Institute · USUniversity of California, San Diego · USUniversity of Washington · US

Funding

VOLUMETRIC CONTOUR-BASED SURFACE RECONSTRUCTIONP41RR004050 · NCRR · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI PASQUALE, ELENA B · 1989 to 2011
$28.0M
Project# 4: INTERACTIONS OF ANCHORING PROTEINS WITH THEIR TARGETSP01DK054441 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TAYLOR, SUSAN S. · 1999 to 2017
$27.3M
IVEM and Image Analysis ResourceP41GM103412 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ELLISMAN, MARK H · 2012 to 2019
$17.9M
Contemporary Approaches to Cancer Cell Signaling and CommunicationT32CA009523 · NCI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DONOGHUE, DANIEL J, YANG, JING · 1985 to 2025
$12.1M
NCI NIH HHS T32 CA009523NCRR NIH HHS P41 RR004050NCRR NIH HHS P41-RR004050NIDDK NIH HHS DK54441NIDDK NIH HHS P01 DK054441NIGMS NIH HHS P41 GM103412
6 · The paper itself

Abstract

Although RII protein kinase A (PKA) regulatory subunits are constitutively localized to discrete cellular compartments through binding to A-kinase-anchoring proteins (AKAPs), RI subunits are primarily diffuse in the cytoplasm. In this paper, we report a novel AKAP-dependent localization of RIα to distinct organelles, specifically, multivesicular bodies (MVBs). This localization depends on binding to AKAP11, which binds tightly to free RIα or RIα in complex with catalytic subunit (holoenzyme). However, recruitment to MVBs occurs only with the release of PKA catalytic subunit (PKAc). This recruitment is reversed by reassociation with PKAc, and it is disrupted by the presence of AKAP peptides, mutations in the RIα AKAP-binding site, or knockdown of AKAP11. Cyclic adenosine monophosphate binding not only unleashes active PKAc but also leads to the targeting of AKAP11:RIα to MVBs. Therefore, we show that the RIα holoenzyme is part of a signaling complex with AKAP11, in which AKAP11 may direct RIα functionality after disassociation from PKAc. This model defines a new paradigm for PKA signaling.

Indexed as

Multivesicular BodiesA Kinase Anchor ProteinsAmino Acid SequenceBinding SitesCatalytic DomainCyclic AMP-Dependent Protein KinasesGene Knockdown TechniquesHEK293 CellsHeLa CellsHumansIsoenzymesMolecular Sequence DataMutationProtein BindingProtein TransportSignal TransductionAKAP11 protein, humanA Kinase Anchor ProteinsCyclic AMP-Dependent Protein KinasesIsoenzymes

Identifiers

PMID21502359
PMCPMC3080257
OpenAlexW2148801773

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.